B-RAF/LOXP-FLANKED MUTANT MOUSE
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UCLA Technology Available For Licensing |
BACKGROUND:
B-raf is a member of the Raf family of intracellular signaling proteins, which also include Raf-1 and A-raf. Members of this family are involved in the all-important cellular signaling mechanism known as the Ras/Raf/MEK/ERK/MAPK signaling pathway. This ubiquitous pathway relays signals from outside the cell into the cell's nucleus, regulating activities such as gene expression, differentiation, cell division, cell survival and cell death. B-raf regulates vital functions in the brain, testes, skin and bone marrow, and mutations in B-raf are found in malignant melanoma, certain types of thyroid and ovarian cancers, and sporadic types of colon cancers. Up to 6% of all human malignancies may harbor this mutation. Most recently, Sorafenib (Nexavar), which inhibits raf as well as a whole host of other signaling proteins, has been approved by the FDA for the treatment of advanced cancer of the kidney (clear-cell renal cell carcinoma).
INNOVATION:
UCLA researchers have made a B-raf/loxP-flanked transgenic mouse. Flanking the B-raf gene with the loxP sequence allows targeted excision of the B-raf gene only when the cell expresses the protein Cre. This allows selective deletion of B-raf in a cell or tissue-specific manner and in a time or developmentally-specific manner as well.
POTENTIAL APPLICATIONS
- Cancer research involving the Ras/Raf/MEK/ERK/MAPK signaling pathways
- Research into learning and memory, and hematopoiesis and myelopoiesis
ADVANTAGES
- Uses proven Cre/LoxP DNA recombination technology for targeted gene excision
- Unlike knockout mutants with global B-raf deficiency, B-raf/loxP sequence allows deletion of the B-raf gene in a cell or tissue-specific manner
- Unlike knockout mutants, B-raf/loxP sequence allows deletion of the B-raf gene in a time or developmentally-specific manner, such as after tumorigenesis or transformation
- Allows functional testing in specific cell types without the confounding effects of deleting B-raf in unknown or unrelated cells and tissues
Related Papers (Selected)
1. Chen AP, Ohno M, Giese KP, Kuhn R, Chen RL, Silva AJ. "Forebrain-specific knockout of B-raf kinase leads to deficits in hippocampal long-term potentiation, learning, and memory". J Neurosci Res 2006; 83: 28-38
Reference: UCLA Case No. 2006-215
For additional technical details and current licensing
availability,
please contact the following UCLA office:
UCLA Office of Intellectual Property
11000 Kinross Avenue, Suite #200
Los Angeles, CA 90095-7231
Tel: 310-794-0558 Fax: 310-794-0638
email: ncd@research.ucla.edu
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NCD URL: http://www.research.ucla.edu/tech/ucla06-215.htm
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UCLA Technologies Available for
Licensing
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Copyright © 2007 The Regents of the
University of California.
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